Why the study?
Does Endothelin (ET-1) induce or modulate aggregation of human platelets in vitro?
Does Endothelin (ET-1) induce or modulate aggregation of human platelets in vitro?
Endothelin-1 lacks a direct effect on human platelet aggregation in vitro, unlike several other endothelial-derived vasoactive agents.
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ET-1 lacks direct effects on human platelet aggregation in vitro; leaves open its potential in vivo or clinical role in thrombosis.
Endothelin (ET-1) is a recently discovered endothelial-derived peptide with pronounced vasoconstrictor activity. The present study addressed whether ET-1, in analogy with several other vasoactive agents, can induce or modulate aggregation of human platelets in vitro. Venous blood from healthy donors was collected in citrate or heparin and platelet-rich plasma (PRP) was prepared. Portions of the PRP were added to drugs, and platelet aggregation was recorded according to Born & Cross (1963). ET-1 added to the PRP (final concentrations 1-100 nM) did not induce aggregation of platelets, either in citrate- or heparin-containing plasma. Adenosine-diphosphate (0.5-2 microM) or thrombin (0.1-0.4 NIH units ml-1) induced dose-dependent aggregation of platelets in citrate- or heparin-containing PRP; such aggregation was, however, not affected by ET-1 (1-100 microM) either. We conclude that ET-1, in contrast to other endothelial-derived vasoactive agents, lacks direct effect on platelet aggregation in vitro.
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Edlund et al. (1990) studied this question.
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